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*
Department of Clinical and Experimental Medicine, Padova University School of Medicine, Padova, Italy;
Institutes of General Pathology and
Department of Pathology, Verona University School of Medicine, Verona, Italy;
§
Research and Discovery LeukoSite Inc., Cambridge, MA 02142; and
¶
Infectious Disease Unit, Massachusetts General Hospital, Department of Medicine, Harvard Medical School, MA 02129
The accumulation of T cells and monocytes at sites of ongoing
inflammation represents the earliest step in the series of events that
lead to granuloma formation in sarcoidosis. In this study, we evaluated
the pulmonary production of IFN-inducible protein 10 (IP-10), a CXC
chemokine that stimulates the directional migration of activated T
cells. Striking levels of IP-10 were demonstrated in the
bronchoalveolar lavage (BAL) fluid of 24 patients with pulmonary
sarcoidosis and lymphocytic alveolitis, as compared with patients with
inactive disease or control subjects. A positive correlation was
demonstrated between IP-10 levels and the number of sarcoid
CD45R0+/CD4+ cells in the BAL. Immunochemistry,
performed with an anti-human IP-10 polyclonal Ab in lymph nodes
displaying prominent sarcoid granulomas, showed that cells bearing
IP-10 were mainly epithelioid cells and CD68+ macrophages
located inside granulomatous areas. Macrophages recovered from the BAL
of sarcoid patients stained positive for IP-10 protein. Furthermore,
alveolar macrophages isolated from sarcoid patients with T cell
alveolitis and cultured for 24 h in presence of IFN-
secreted
definite levels of IP-10 capable of inducing T cell chemiotaxis.
Interestingly, alveolar lymphocytes recovered from patients with active
sarcoidosis were CD4+ T cells expressing Th1 cytokines
(IL-2 and IFN-) and high levels of CXCR3. Taken together, these data
suggest the potential role of IP-10 in regulating the migration and
activation of T cells toward sites of sarcoid inflammatory process and
the consequent granuloma formation.
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